We have been working on the molecular basis of transformation by simian virus 40. We have confirmed that viable deletion mutants which produce no little t antigen are defective in transformation when confluent cells are treated with virus. On the other hand transformants produced in rapidly growing cells and selected either by their ability to form foci on plastic or to grow in soft agar are indistinguishable from wild-type transformants. It has recently been demonstrated that SV40 can cause transformation in two ways, distinguishable only when the virus contains a temperature-sensitive mutation in the big T antigen. We have therefore constructed temperature sensitive mutants which also contain viable deletions and are currently characterizing cell lines transformed by these double mutants. A working model has been devised.